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Reading Royal Bucks or Hospital in the Thames Valley Dean Ary. And um thank you so much for having me today. I appreciate you've had a long day of lectures. Um So hopefully I'll try to keep this as concise as possible. I think the aim of the session is not really to go into like the tiny details of um the physiology of things. Um Obviously, there'll be some of it, but I think most of it would be just going through some high yield topics and some practice questions for your biology exams as well as just being familiar with a structure that will help you approach the questions in the exams. Okay. So um what we will cover today is electrolyte imbalances. So mainly sodium potassium, calcium acid base back acid base balance as well on knowing how to be a BGS and interpret them and then liver function test. So when you become an F one doctor or you know, F two as well, these are some of like the commonest things you do literally every day on your job. So that's why I sort of like Campath because I find it one of the more applicable to one of the topics that are more applicable to your class medical practice. Um So yeah, hopefully you will find this talk beneficial to. So, first of all, we will go through sodium and fluid balance. Um I think there is a bit in the beginning where um we were taught sort of oz morality and osmolarity. Um in clinical practice, there is no really um uh sort of um you don't really need to know which one is more uh so relevant clinical practice, the the important difference for you to know is that one of it, the osmolality is based on mass of the solvent, whereas osmolarity is based more on the volume. So say, for example, um on the wards, you're asked to take blood from someone, do you think it would be easier to take a blood or calculate blood based on the mass of the sample that you take or the volume? So clearly is the volume, right? So the important thing for you to remember to take away from this is that in clinical practice, what we normally you look at, it's osmolarity rather than osmolality. So you don't have to worry too much about osmolality because you don't really won't really encounter this um in real life, it's more about osmolarity. So just remember that osmolarity is based on the volume of the solvent and it's calculated from the blood test that you do. And um however, in your exam, they do want you to know how to calculate or small al itty and what the formula for this is. So this, I'm sure you must have seen. So it's two times of sodium and potassium plus glucose and urea and the normal range should leave it 22 75 to 2 95. Now, why is it, that is two times of sodium and potassium. This is because the amount of positive ions that you have in your blood is should equal the amount of negative ions. So therefore you times that by two. And um sometimes if you find that whatever it's measured in the lab, if it is higher than your calculated or similarity by more than 10, then that usually means that there are other substances present, there are not part of this equation. So that is not glucose and not urea and not you're positive ions. So things like alcohol, sugars and lipids and your proteins that may also be present in blood. Okay. Just so take home message for this is you don't really need, you don't really use osmolality in clinical practice and um not really bother about the difference between them. And sodium is the largest contributor to your plasma osmolality. Sodium. Um the level of sodium in your blood, you're looking at between 135 145 potassium, usually between 3.5 to 5 or 5.5 is usually quite acceptable. Okay. So jumping on to um the I hope you still have this format of question. I think you call it clinical prioritization question in your pathology exam. So remembering the equation for osmolality that we encountered just now. So two times of sodium plus potassium glucose per syria based off of that equation, can you now, I'll give you some time to rank these conditions and order of your highest similarities lowest. So it should be osmolality, not osmolarity. That is a type of apologies. Um Yeah, so I'll just give you some time and I think I can look, yeah, I can look if someone wants to type in the chat as well. What you think the answer is then that will be good and it will go through the explanation. Hatred test is fires very good. If you want to type in your reasoning as well, that would be excellent. And just thinking along the lines of Petri Hs, what do you think could be the second highest um hospitality? Okay. So I'm just gonna assume everyone has had time to think about this. I'll just move on to the answer. So um number one highest hostility is hate, hate, hate H H S the out to date term is called Honk, which basically is um hypoglycemic hyper or smaller or smaller um nonketotic coma. They mean the exact same thing. And um number two is D K A number three diabetes, insipidus pneumonia S I D H. So just to go through explain to them. The diagnostic criteria for hatred S is that you need to have an osmolality of more than 320 usually is patient's who come in with this. Um They are type two diabetics, they are profoundly dehydrated. So they're osmolarity would be really hi. And by definition, it is above 300. So yes, that's the one of the highest similarity. Secondly, of diabetic ketoacidosis because you remember in the osmolarity equation of glucose, that forms part of the equation. And in DKA obviously have raised glucose. Um and usually someone with type one diabetes could be a first presentation of type one diabetes. So they have raised glucose. Therefore, second highest similarity, not as high S H S. So thirdly of diabetes insipidus, if you remember, this is a condition where you either have absolutely no ADH production, which is cranial diabetes, insipidus or you can have uh nephrogenic diabetes insipidus where your um renal collecting ducts, cells are not sensitive to the ADH, therefore, resulting in less water re absorption. Therefore, your osmolality would be sort of quite high up as well in pneumonias. Why is this relevant? That's because sometimes um pneumonia can lead to S I D H, not old cases and it's not very common but that can happen. However, in S I D in as medicate, you have a clear increase production in ADH causing your excess water absorption. Therefore, out of all of those conditions, it will have the lowest of similarity. Okay. So this would be the most likely ranking of the conditions, the price, lowest hospitality. Okay cool. So that is we've got a similarity out of the way. Now let's look at sodium regulation. Sodium is most um linked to water because it is the amount of sodium that you have, it is dependent on the amount of A D H that is produced. So say if you have just talking about how sodium is regulated first, so you have increased blood volume. What this will, what will happen is you can have stretching of the cells in your atrium. So H O stretch and then this will then lead to increased the release of your HL natural natural retic peptide. At the same time. What will happen is you've got your re Renan angiotensin aldosterone system involved as well. So this will lead to a decrease of your aldosterone, also your ADH and your Renan. So overall you have a decreased sodium concentration and your blood volume when you have an increase in your blood volume. Okay. Now, thinking about sodium regulation and how it plays a role in osmolality. If your blood is concentrated, say if you're dehydrated, you're thirsty, what will happen is your hypothalamus would um respond to this by integrating ADH release. So therefore, with increased ADH, you have more water that's re absorbed and therefore your decreased sodium concentration in conditions where you have low odds morality. So, the opposite happens, your blood doesn't want more water. So it will suppress production of A D H by hepatal A muscle and then you will increase your sodium concentration. Now, there is a conflict that occurs that can in the role of a th if state we have both low blood volume and low osmolality. So an example for this would be say, a patient who has high Paavo limit hyponatremia, which we'll get onto it a bit later. In this case, we what will happen is the the blood, maintaining blood volume, Trump's maintaining the oz morality. So, maintaining blood volume is more important and therefore ADH will increase in this indeed in these instances, even though you're osmolality is a bit low because um your body wants to preserve that blood volume. Okay. Now, in hyponatremia, which is the commonest, commonest electrolyte imbalance you will see in clinical practice, the number one thing you need to first do when you see say a sodium of like 100 29 what would you do first? So the first thing is you need to make sure it's not a condition that what it's called pseudo hyponatremia where you have low sodium, but normal or high plasma are similarities. So example would be if there are other substances present in your blood. So things like high lipids, high proteins in for instance, like myeloma or high sugars like in diabetic people or alcohol. Okay, once you have excluded pseudo hyponatremia. Then you can say okay, the patient has true hyponatremia. Now, what is the next step? Then you should then do and Amir Sam I think probably has a set this multiple times. What do you need to do? Assess the fluid status? Okay. So the next thing you need to do is then what it's just think about in real life as an F one. When you see this blood test 128 109 sodium, what do you do? Look at the patient, examine the patient? Are they in a hypo bulimic state or are they in a hyperbolic nick state? Or do you think that just, you know, you will email so things to look out for would be like observations. So looking at the BP, looking at the heart rate, if there are hypo bulimic, then obsolete BP was a bit low. They, their heart might be a bit Tacky Kartik, the cat refill might be a bit prolonged if they are hyperbole mix. So, you know, they've got blood in there, extra vascular compartment. So they will have peripheral edema, pitting edema sometimes and you could hear by basal crackles as well in some instances of pulmonary edema of patient's with heart failure. So once you've assessed their volume status and you're happy that actually the patient seems quite dehydrated and they are therefore hypothalamic. And then you need to think about what could have caused this hyperbole, make hyponatremia and the next investigations you will then request as the F one F two would be um had so serum urine osmolality, but also urine sodium. Now the reason this is a very good uh test that helps to point you towards like what possible cause it is is if your um urinary sodium is high, what this means is your kidneys are failing to do its job in retaining the sodium. Because remember when you retain sodium, then you also increase water absorption and then you increase your blood volume, right? So if you have a high sodium in your urine, it means your kidneys are not doing the job. So therefore, that means that it is renal losses. Okay. So things like chronic kidney disease, the patient maybe on direct ixis or so variable salt wasting you, it's just, you know, academic, you don't really see it in real life, but I've just added it on because it's taught in our lectures. Um if the urine sodium on the other hand is less than 20 then you know the kidneys are doing their job. So the kidneys are desperately trying to hold onto the sodium to help maintain your blood volume, which means the uh sources of your loss of your water is other organ systems. So uh from the gut, for instance, if your form it saying if you got got diarrhea or from your skin in patient with burns, okay. So the management for this actually really simple treat. The underlying course, if they've got diarrhea, then make sure they're direct resolved. If appropriate, give them some of the paramount if um they are a bit uh dehydrated, then give them some IV Saline. No 0.9%. Um Hypertonic Saline. I have never actually had to prescribe this and usually medics are very hesitant to prescribe this because patients who need hypertonic saline will have to be transferred to um the higher monitoring unit. So it's not usually prescribe on just your normal regular medical wards. Um And what it's normally prescribe only if patient's are symptomatic. So say if they have like seizures or like acute drop in the G C S, um then you would prescribe hypotonic saline. But otherwise, usually we just prescribe normal appointments and saline. Okay. So that's hypo believing hyponatremia, hyperb olympic hypernatremia is when you have um your total amount of water in your body is high. However, you have low effective arterial volume. What this means is that the amount of blood that's circulating around your body is not say good enough enough to supply the perfusion of your organs. Okay. So, this would occur in conditions with reduced cardiac output like cardiac failure or if you have um increased peripheral arterial basal dilation in patients with liver conditions, cirrhosis where you you delivers unable to break down the vasodilators, which is why if it's just thinking about how this is applicable in clinical practice. Um If patient's have cirrhosis and they have like, you know, upper gi bleed and you're suspecting a virus you bleed, you give, tell a person because tell a person helps to basil constrict. And that's because in cirrhosis, you're unable to break down the basal like dilators causing peripheral artery vessel dilation. Okay. And so again, what do you do? Check your urinary sodium? Because it tells you what the likely underlying course is. If it, the urine sodium is more than 20 then again, kidney is not working. So chronic kidney disease, if it's less than 20 then it's other um other conditions. So like chronic heart failure, cirrhosis. Okay. So management treat underlying course and very simple because they're hyperbole Mick, they have large volumes of water. You just need to fluid, restrict them. And normally um they, the sodium levels tend to come down quite nicely. Even if you just place them on like 1.5 liters depending on how severe it is one liter to 1.5 liters per 0.4 hours, then normally the sodium would be able to improve okay after a few days. Now, if you are happy that the fluid status actually euvolemic, normally the course for this would be endocrinological causes. Okay. So um things like again, spirit before we go into the causes check urinary sodium okay. And um the reason so because this is due to endocrinological causes most likely before you say that it is SIADH, you need you absolutely need to request other um endocrine blood test. So if a patient say yeah, you think the hypo euvolemic and they have low sodium, the the seniors on the water, the med brand, for example, would be quite happy if you say okay, my next investigation, my next test to add on would be thyroid function test or a early morning cortisol. And then like uh so this, this f one knows what they're doing, you know, they know that you really make. Therefore, you need to exclude other endocrine causes before you say okay, this patient might have SIADH and we'll, we'll go on to S I D H in a bit. Management again, treat the underlying course. Um In some elderly patient's, they don't really eat much apart from, you know, drinking tea and toes and that could cause hyponatremia. Um So just giving them a more uh better diet with like more macro nutrients, supplementing them with like end shows. Again, fluid restricting them usually works quite well as well. Demeclocycline and 12 Acton. I have not personally seen this prescribed on some of the wards that I've worked in. I've mainly worked in elderly care. Um I think some endocrine uh wards or red shots, they do prescribe it, but it's a very expensive drug. So I don't think it's prescribed very much at all, but in cases of resistant SIADH, just so for your, for your own knowledge, these are some of the drug options um to treat patients who don't respond to fluid restriction. Now, diagnosing S I D K H some of the causes um that are common would be things related to your brain, um uh the lung and pills. So in brain, it will be things like um uh two brain tumor, craniopharyngioma for angioma, um lung, things like pneumonia or like um lung cancer and then pills some um drugs that can cause that will be things like SSRI very common PPI proton pump inhibitors, um carBAMazepine opioids, dopamine, and taglines, etcetera. Okay. So again, S I D H, you can't just uh diagnose it there and then like say low sodium, you will limit, oh it's s idea that you can't, you need to exclude other endocrine causes first. And the diagnose the criteria for S I D H is important for you to remember this because you will then know what blood test to send off. So you need to send um obviously use the knees with your sodium. You need to send your pet serum and urine osmolality. So they come together and then you have your urine sodium, it has to be high. And then as I said before, you need to exclude all other any crackles. So no, no adrenal thyroid dysfunction that you suspect. Okay. So this is just a flow chart that I find quite helpful when thinking of what could cause hyponatremia. Then when you're as an F one I So I definitely found this like useful. So feel free to take a screenshot or if you want to look back to recording, you can just refer to this flow chart. Okay. Um Right. So take a message hyponatremia as a water problem before you think about what could cause hyponatremia. Go and examine the patient, determine the volume status. And S I D S I D H is a diagnosis of exclusion. We have to exclude other eloquent causes first. Ok, hypernatremia. Uh nothing is not, nothing much to say about hypernatremia because hyponatremia is a lot more common, but hypernatremia definitely exists in patients who are a bit more dehydrated. But your approach would be exactly the same as in someone with hyponatremia. So first of all, assess the volume status. Do you think they're hypo or hypervolemia? Okay. Okay. And in management, usually we just encourage patients to drink a bit more. So in our plan encourage oral intake, make them drink a bit more water, nurse to encourage oral intake. Or um sometimes if it's still not coming down, maybe some patients with dementia, they just don't really eat or drink much without prompting, then you can supplement with some IV fluids. So that will be with IV Dextrose or obviously you don't want to give them more Saline because in no 0.9% saline, you may be aware, it has like 100 54 millimoles of sodium. You don't want to give them more and then guided by urine output and plasma sodium. You don't want to um make the sodium levels drop too low, about 10, 8 to 10 million moles per 24 hours. It's a good um is a good age, a good guide. Okay. Um Right. So diabetes insipidus, hers is the opposite of anxiety age. I think we've touched on this a little bit earlier on. So it could be either central causes where you, your brain just does not produce your anti directed hormone or nephrogenic causes where it's resistant to it. Okay. So these are just some of the causes. I'm not going to read them. I'm sure you double your own. Um And to be honest, it's not very common at all in clinical practice, I've probably only seen um one once or twice, but even then it's more like lithium induced. Um But anyway, so key investigations before you um say that this patient either has cranial or nephrogenic diabetes insipidus, you need to exclude the very common conditions first. So do a blood glucose level to exclude diabetes mellitus. Do your user needs to exclude high hypokalemia. You need to do a bone profile as well. Looking at your calcium to exclude hypercalcemia and then you need to do a plasma and urine osmolality. And then finally, water deprivation test, okay to diamonds, diabetes insipidus. Just looking at the interpretation of the water deprivation test. If you restrict a patient from drinking water and the urine actually concentrates. Then that means that they're not having any, you know, abnormal condition or it could just be primary politics. There were just, just drinking way too much water. If the urine concentrates after you give them decimal present, then this means that because remember, desmopressin is a, it mimics the action of your endogenous ADH. So if your urine successfully concentrates after you give them desmopressin, then this means that their brain cannot produce them. Therefore, it's a central cause. However, if it remains dilute after you give them, there's no present, then it means that the kidneys can't respond to it. So it's a nephrogenic course and the diagnostic criteria, this is important to know is that despite race plasma or similarity, your urine is still very dilute with the urine plasma, osmolarity of less tectorius 31. And that is for your diagnostic criteria for diabetes insipidus. All right. So let's have a look at this um V S A question. So you have a 65 year old gentleman, long term smoker. So the thing about to remember about exams, every single thing that they include is an, is an important piece of information. Okay. They rarely ever include red herring. Okay. So long term smoker presents with a two month history of cough, shortness of breath and weight loss examinations are remarkable. Um now you've given some blood tests, you've got sodium of 1 to 8 huh bit low, not, not too low but bit low potassium is normal four adjusted calcium 2.4. That's also normal 2.2 to 2.6 is normal urinary sodium of 40. Okay. Normal th TSH and Cortisol level. Okay. So you know the endocrine problem, he doesn't have any endocrine issue. What are the what in the, in this results or jumps straight at you or what could help you point towards what the diagnosis might be? Chest X ray report is pending as always in hospitals like radio, just never really prioritize reporting chest X rays except if it's for like N G tube placement. So usually takes at least a few days before the report is out. What is your next best step in investigation? Okay. Actually, this is a two step question. What do you think they're trying to allude to and then what is your next best step in your investigation? Yeah. Yeah, good. So someone said S I dish for lung cancer. Yes. So, you know, they gave all your red flag symptoms of cancer long term smokers. So you're thinking of lung cancer and could just be S I D H. And I guess it's helpful that they gave urinary sodium of 40 because it means that the kidneys are not, are also not working, working very well. So this patient might have, you know, a concurrent kidney issue, but it's likely pointing towards S I D H from lung cancer. So what is your next best step. If you think it is SIADH, you know, they're true, assess successful it states is very good. However, the questions asking for a test when you assess for it stays more like examination. Yeah. So water deprivation test is for diabetes insipidus. So that's the opposite of S I D A D H when you can't, where you can't produce A D H. Um But yes, pad um, osmolarity is correct. Pet serum and urine osmolality is you've already got the urinary sodium results. That so is what fits one of the criteria for your SIADH. And you need to figure out whether it meets the rest of the criteria. So pad serum urine osmolality. So in SIADH, remember, but that your urine soldier has more than 20 your plasma osmolarity has to be less than 270 your plasma sodium has been less than 100 35. So actually already he meets one of he meets the plasma sodium criterion as well. And also apart from that, you need to have high urine osmolality of over 100. Sorry, just was okay. Sorry. I thought that was a question. Fine. Okay. So if everyone's happy with this, let's move on. Uh take home message through hypernatremia always means hyper high possibility because your sodium makes up the most part of your hospitality equation and diabetes insipidus is excluded if your urine and plasma similarity ratio is more than two is to one because remember has been less than two is to one. Okay. Um Does everyone, is everyone following so far? Okay. With sodium, that's the commonest, you know, electrolyte problem. You see and then potassium is the next one. OK. Is everyone happy for me to continue to potassium? Okay. I'm just gonna continue. Right. So potassium now thinking about low potassium, um the patient's might present with, in fact, most of the patient's with incidental finding of hypochelemia. When you do like your user knees on your, your blood test on the ward is they don't really have any symptoms. But in in situations where the potassium is quite low, patient's may present just being complaining of the general fatigue, just complaining of some muscle cramps that quite nonspecific um E C G features of hypokalemia is basically opposite to the of hyperkalemia where you have flattened T waves rather than tall tented T waves. Um But importantly, you have prominent new waves, okay and also prolonged pr in total causes of hypokalemia will be things like increased loss of potassium, um increased cellular influx and decrease intake. So just going into a bit more details about different causes. Um potassium loss would be commonly things like loss from your gut or your kidneys if diarrhea, vomiting, high output stoma, um renal losses, things like Khan syndrome. Actually, to be honest, I should put director X first because that's way more common um direct IX. And then think about other more rare conditions like con syndrome, congenital defects, increased cellular influx. Now, this is very common. So, essentially iatrogenic causes if the patient's on insulin, if you're prescribing, um some patient with beta agonist. So commonly things like salbutamol in an asthmatic patient, if they have re feeding syndrome, causing shifting of your potassium cells and forced weight cells, etcetera into the cells and then um metabolic al pelosis. So remember potassium goes hand in hand with hydrogen, which I'm sure you might remember for your campus fractures. If it is low potassium, then that causes a low hydrogen as well due to the exchange of the hydrogen potassium ions that occurs at the cellular level. Um So in the case where you have low potassium but high hydrogen ions or acidosis, then you think about like very rare conditions like reno tubular acidosis and sometimes partially treated decay. But remember low potassium comes hand in hand with low hydrogen and high potassium high hydrogen islands. Okay. So high potassium acidosis um ki investigations, this is one thing that's important to know for clinical practice as well. If a patient has low potassium, you will want to check the magnesium level and you will always replace your magnesium together with your potassium because it just has some nothing to do with. I'm not sure what the details of it exactly are the physiology behind it. But essentially if you um if you supplement the potassium before supplementing that magnesium, then it wouldn't quite work. You need to supplement both of them. If both of them are low. If a patient is quite young, they have high BP, then you might want to think about something going on in their adrenal. So you want to check. So things like Khan syndrome, you want to check the aldosterone rent and ratio. How do you manage low uh potassium? Very simple. If it is to be fed, this varies. Um depending on your trust guidelines. So what I would do is basically all hospitals should have guidelines on like what are the thresholds for when you should supplement orally versus when you should supplement IV. But if it is mild to moderate, um I would say my, my current trust actually is like 2.83 point five, then you prescribe orally sand, okay twice a day for three days and then just do repeat the potassium in three days time. If it is severe, then you will want to give them IV. So um 10 millimoles per hour is a good gauge. Um In my trust, we don't prescribe anything more than 40 millimoles um in the day. So IV, potassium chloride, this can be given on the wards. Um doesn't have to be in the higher monitoring unit, but they do need to have E C G monitoring or just cereal bcgs just to make sure there's no E C G changes and check the using these daily in all cases just to make sure that it is um the potassium is resolving or improving in hyperkalemia. I'm sure very familiar with this. So finding E C G features you get, you can get asked about this in finals in the acute care stations. For instances you get told tend to T waves, a small P wave one in Q R S prolonged pr and in very severe cases, you can have a sine wave leading to avenge particular uh fibrillation causes artifact causes iatrogenic, reduced excretion, increased cellular release. So just going to a bit more detail artifact would be like if the blood cells just himmel ized um iatrogenic. If the patient receives um say like a couple of units, a blood transfusion that can cause the potassium to go up a little bit. And if you get excessive potassium therapy and like Casey or like um normal saline with added uh potassium in reduce excretion. Normally cases where your kidney is not functioning very well. So, renal disease, aldosterone deficiency or drugs, um protest inspiring diuretics and increase a cellular release. So, um as I said, hi, protesting comes hand in hand with high hydrogen, so metabolic acidosis or if your tissue breakdown. So um in patient's with, say if they've had a fall with the long line, you think about rhabdomyolysis and then you think about high potassium as well. Okay, key investigations definitely um renal function. You need to check A C K as I said in, in instances where you might suspect rhabdomyolysis, um, quote, so level, I wouldn't really, I mean, I don't think we would do that. So the day to day practice also quite an expensive test. But if you're suspecting an endocrine courses, then yes, your um, the registrar consultant might, might suggest you to do that and um treat if you see E C G changes or protesting more than 6.5. Again, this varies depending on your trust that you work in, in my trust. We treat if it is 6.5, it is sorry if it is above six and if there is any changes or if it is above 6.5, okay. But the manage the initial management that you do for hypokalemia basically is the same throughout you give IV Council gluconate. If their A C G changes to protect the heart, you give IV insulin with dextrose. The reason you give insulin is if you remember insulin helps to drive potassium into your cells, so it doesn't sit in your blood and your circulation. So causes helps to improve the potassium level, but also dextrose because obviously when you give insulin, then you can bring the blood sugar down sugar levels down. So you need to supplement that with some dextrose. Um in some instances, say for example, might take a bit of time for the nurses to set up the IV insulin or to get the IV calcium gluconate from pharmacy. So you can just in the meantime give them some nebulized salbutamol actually works quite well. Um And then potassium binders, I think now we learn about calcium Rizzo knee. Um but I think that's a bit out of date. Now, what some trust now use or in fact, most trustees now is Lokelma. So that's um sodium. I don't remember the full name sodium zirconium cycle. So something like that, but essentially what it does is um it is a potassium binder. So it binds to your potassium in your gut and that increases your potassium secretion from your urine. And obviously, if it is um if you remember one of the indications for dialysis is refractory hyperkalemia. So say if you notice that patient's after like maybe a few rounds of IV insulin and dextrose, they're still not improving after maybe like 30 40 units, then I might think about escalating this to I two. In which case, they may come and assess the patient and say whether and decide whether they fit for dialysis to help solve the refracturing hyperkalemia. Um All right. So take a message if potassium is low, remember to check magnesium as well and supplement both at the same time. If magnesium is also low, if potassium is unexpectedly high, say maybe yesterday it was like perfectly normal and then suddenly today is like over 6.5 or seven, definitely repeat first before treating and how because blood tests in real life takes a couple of hours at the very least, even if you send it off as an urgent blood sample. So what would be quicker is actually just do a V B G, just do a V B G, run it at a blood gas machine and then you can get a reading of the potassium level quickly within like you know, a minute or two. So definitely do a V B G but also send a form of blood tests for the formal potassium level. Okay. So now um if we look at this S B A, you have a gentleman, 50 year old considered quite young uh with known hypertension attends an annual review at his G P. He takes Ramipril 10 mg once a day. His blood pressure's 100 38/78 his a symptomatic and feels well. His foot test results are as follows. So sodium 139 potassium 6.8, you were five correcting 90 E G F R 88. Mm. What's the most appropriate immediate Axion? Is this BP fine? So rise in it since historic, less than 140 that's all it, less than 90. He feels well taking Ramipril but in the blood test, renal function's not too bad, but then he knows this 1006.8. What do you do? It's you know, it could be likely very likely a spurious result. So therefore you want to before you do anything or make any changes to the medication, you want to just quickly repeat the use enemies. Okay? Because you think, you know the patient's, well, everything is fine examinations. Okay. What's the potassium so high? You just repeat use any before you reduce, before you choose to reduce the dose of Ramipril. I think there is a threshold where say it is a real hyperkalemia. Obviously, Ramipril causes that. So um I can't remember off the top of my head. How many percent of like a rise in your potassium in where you that would indicate sort of like a reduction in your dose of ramipril? Um I would check the nice guidelines for this but essentially six point is quite high. Everything else is, you know, green flags. So I would repeat the you Zinni's okay. Second one, a patient has had hypertension at a young age. So we're thinking maybe like less than 45 less than 40 or around 40 and following blood test results on this use and ESRs follows sodium of 147 protesting three point to your ear of five. Correction is 70. What is the next best investigation too? So you need to rediscover feli. It says to confirm the likely diagnosis. What are we thinking for someone young hypertensive race, sodium, low potassium. Yes, good. So I've just seen someone has said Rendon androsterone ratio. Yes, because what we're thinking of in this case is a con syndrome. So in which case, aldosterone random ratio would be the next best investigation. So remember it says next, it's not like um the diagnostic invest and then if it is a di diagnostic investigation, that obviously will be a form of imaging, so like a ct scan of the adrenals, in which case, it will show like you know a mass which points towards adrenal tumor could be cons okay. But next best investigation will be aldosterone random ratio which could be obtained from your blood test. Okay. Okay. So that is your potassium and then we'll move on to the next commonness of electrolyte imbalance that you encounter. Clinical practice. Calcium. It will will go through a bit of calcium physiology first and the vitamin D because that's actually it comes out quite a lot. And once you understand physiology, you will know how to like treat them and know how to interpret the various blood test. Okay. If everyone's happy for me to continue, I would just carry on. Okay. Now, calcium, 99% of it is found in your bone, the rest of it is in your blood. So it's either in the free form where it's ionized or it's bound to album in or it is complex with other ions like side traded phosphate. Don't really need to know absent itches mainly just know that it's most of it or in fact, almost all of it is a bone. Okay. Now, um paradigm thyroid hormone. Um two main hormone, sorry that you need to know paradigm parathyroid hormone and your calcitonin. Okay, parathyroid hormone. What does it do? It increases your serum calcium and decreases your serum phosphate. But calcitonin does the exact opposite. And these two hormones act at three different organs in the bone kidneys and your gut. Okay. So there is what happens with P T H is you have increased bone resumption by osteo class, decreased phosphate reabsorption at your uh your kidneys and your calcium in also in the kidneys. And then you have overall less calcium absorption in the gut. And then the opposite happens in calcitonin. Okay. The important thing you need to remember is that vitamin D is important to facilitate the absorption of calcium. Okay. And the active form of vitamin D is calcitriol. Okay. What happens if you have low calcium level? So the kind of symptoms uh the patient may complain with or even signs that you may see commonly um parasthesia. A arrhythmia is when you're getting a bit like okay. This is not looking very good but definitely escalate to the seniors. Um convulsions again, not great. Patient needs to be seen by our to you if they have a tetany or spasms and these are the salt um that the names for it. Uh social sign is virostek sign. Some causes low parathyroid hormone levels. So in conditions, congenital ones like the George syndrome, commonly after thyroidectomy. In which case, that would be secondary hyperparathyroidism or you can also have low magnesium levels causing that. And then obviously vitamin D deficiency commerce course of hypocalcemia. Okay. Um laryngo spasm just, just so you're aware is a potentially fatal result of hypocalcemia. So let's say you get a scenario where a patient uh post thyroidectomy has been discharged by the surgical team and suddenly comes back to any um presenting with a uh say a horse voice, inability to talk, inability to swallow. The two most important things you need to think about. There are emergencies are number one, laryngo spasm, but also number two, if they might have some sort of uh hematoma from the surgery, compressing the airway. Um, but the reason laryngospasm is more relevant in a post thyroidectomy is because sometimes the surgeons might also accidentally, um, reset your parathyroid, which is, which sits obviously on your thyroid. And actually, you can't really tell the difference at all. It looks like the parathyroid. If you've seen uh endocrine surgery, it literally looks like a lymph node. So it's very difficult to tell the difference. So it's not uncommon for them to accidentally resected. Um And so laryngospasm is potentially fatal and um hopefully you never see it in real life, but if it does happen, definitely, definitely alert your seniors, okay, investigations E C G, definitely you want to exclude Aeneas or for a cardiac signs. Um, and the alarm and cardiac signs are the bloods. So when you depending on which hospital you work in when you request bone profile that very helpfully comes with phosphate, like automatically phosphate calcium and P th. Um you do need to request for LP separately. And also um what's the other one? Vitamin D level that would be separate blood test? But bone profile would be phosphate P T H and calcium. And if the patient's say comes in with the fall, there are very nice um set nice guidelines regarding who we should consider for Dexa scan. So if you're interested, you can look into that. But I wouldn't worry too much because it's like the pathology exam. Maybe more whole final. Yeah. Management wise again. Exactly the same as potassium if it is low supplement with oral calcium. But also remember the commonest cause of low calcium is low vitamin D. So you need to give them vitamin D supplementation at the same time. So normally what we'll give them is at coll where you have both your vitamin D and your calcium. If it's severe where they're symptomatic, then again, IV. Okay. So I haven't covered Force fate in this talk, but for force fate is also exactly same with low phosphate. Then treat them with oral sand. Okay. There's no such thing as oral sandal calcium. There's only sand. Okay. Sorry, low phosphate treat with oral Sando phosphate and low potassium, oral Sandoz. Okay. Uh but calcium is just, there's no sandal calcium. So it's just calcium. Uh Right. And if you're symptomatic, always go IV. Ok, hypercalcemia. I'm sure you're very familiar with this stones. Bones groans, moans. So, these are the signs and they actually do present with these signs. Causes would be in, um, instances where you into pretty blood test. If it's low parathyroid hormone, then you want to think about malignancy most commonly metastatic cancer if it's spread to the bones, um, in myeloma as well, you get hypercalcemia as part of the crab. Remember, calcium or crab, um hyperthyroidism. If there's low uh hypoadrenalism, psych sarcoidosis, thiazide, vitamin D access, all the vitamin D access doesn't really happen much in real life race. P th um in instances where you have primary tertiary hyperparathyroidism. How do you differentiate between these two is in tertiary hyperparathyroidism that's normally very late, late stage CKD where you have autonomous production of your P T H. And and if it is primary, if you remember it forms part of the men, one men to a syndrome. So you want to think about whether they have other signs of like, you know, all of the other conditions that form part of the syndrome as well. So like any pituitary symptoms, etcetera. Ok. Investigation. So myeloma screen definitely, definitely consider if it is a patient um above the age of 60 thorough function test called PSA level management. Remember Mirren says, fluids, fluids, fluids and that's, that's actually how we do it in real life. Little. Just give them. Even if it's 34 liters of fluids, we just load them with fluids. And if you think that their kidneys are not functioning very well, then you can all sorry, their heart not functioning very well. They're not really pumping well. Then you can supplement directives to help diaries them so that you can fill them a bit more with fluids. And then if, if they are fluid refractory, then you can think of moving on to second line medical treatments, things like things like bisphosphonates. Um and Cinacalcet cynical, that's very, very expensive. I've only ever seen it prescribed once. Usually patient's respond to bisphosphonates in case where they don't. Um I've had a patient once he's got undiagnosed of metastatic prostate cancer and unfortunately, had to be palliated because his calcium was just persistently above 3.6. Even though we've loaded him with like, I don't know, probably eight liters of saline and given him three doses of bisphosphonate. Um But as Cinacalcet hardly ever gets prescribed because it's very expensive. And surgical management with parathyroidectomy. Obviously, if it is um in the realm of endocrine surgeons, if they've got a cancer like parathyroid Arjuna, more than that will usually uh go through the enterprise surgeons, the other conditions that can cause um uh to think about in relation to like calcium with Paget's disease where you have, if you remember abnormal bone remodeling. So you have an isolated, raised a LP in osteoporosis. It is not an issue with um production of the bone material itself, but rather the density of the bone. So therefore, you actually have normal calcium, normal bone profile. So normal calcium phosphate and P th it is the volume and density of the bone that's reduced, but the level of your calcium is normal. That's important to remember. Um This is probably in your path book. I would definitely remember this. I don't need to memorize it. I mean, if you understand the physiology of calcium and enforcement and all that, this should hopefully. So make sense to you. It don't, don't memorize it cause just yeah understand physiology and then you know the how to interpret the tests. So now another example of C P Q rank the plasma calcium concentration in these conditions. One sorry, another type of one being the lowest and five being the highest. Let's start with something maybe like easy. What do you think is the lowest lowest calcium level in these conditions? Paratore carcinoma? What happens? Obviously, it's a cancer produces lots and lots of parathyroid hormone. And then paradigm a hormone increases a serum calcium, right? So obviously, that's going to be somewhere along four or five, basically higher calcium level Osteo Malaysia. What is osteo Malaysia? It's when you have lack of vitamin D, right? And remember vitamin D is required for calcium absorption. So if lack of vitamin D, you therefore have lack of calcium as well. So it is you would think calcium is low or simulation osteoporosis. What do we establish normal bone profile? So therefore, it sits somewhere in the middle k likely three. Now, secondary hyperparathyroidism and primary hypoparathyroidism. If we think about secondary hyperparathyroidism, usually it happens in chronic kidney disease, right? And it is raised P T H level, secondary to low calcium normally happens in the short term because in the long run, remember what happens is you get tertiary hyperparathyroidism where you have your autonomous secretion repeat E H. So the level of calcium that is low is sort of more short term. So therefore, it is also slightly low calcium but not as low as say like osteo Malaysia. Okay. In primary hyperparathyroidism, the examples would be things that we're thinking about parathyroid, add normal or hyperplasia where you also get race P th causing race calcium but not as high as like a militant cancer parathyroid carcinoma. Okay. So therefore, the rankings would be the lowest calcium level being Osteo Malaysia because you just don't have enough vitamin D to absorb the calcium, secondary hyperparathyroidism where you have raised P th in response to low calcium in the short term and chronic kidney disease, osteoporosis where your bone profiles, normal calcium is normal primary hyperparathyroidism where you get raised P th um but not as high as stay in a parathyroid carcinoma. It's hopefully this makes sense right now V S A which enzyme is raised in Paget's disease and Osu Malaysia and it's caused by osteoblasts activation. Hopefully, you know the answer to this question enzyme that's caused by yes A LP. Now, the learning point that I want you all to take away from this is for V S A, they want every single answer to be spelled out in full. So you're a LP has to be written as alkaline phosphatase. Okay. They actually will deduct marks if you just write a LP. Just just remember that. Okay. You need to spell everything in full. So say alkaline phosphatase, obviously, they won't ask you for something that is very niche, you know, like enzymes, they want you to spell everything but things like A L P is quite reasonable for you to know the full name. So I would definitely spell out in full alkaline forceful taste. Take a message. Communist course of hypercalcemia in the community is a parathyroid adenoma and the management is fluids, fluids, fluids. So just give them no 0.9 saline or no point in sodium chloride. And see, hopefully they respond commonest cancers that can metastasize to the bone. There are five of them actually. Um but the communist three, our prostate breast and lung, the other two are your thyroid and your kidneys is good to know all five. But these two are the commons. Okay. So if we are happy with uh calcium, we will move on to the next one which I actually really like. And you will interpret every day in your life as an F one as it based balance. Okay. So in interpretation of your blood gas, the first thing you want to look at, I hope obviously is the ph right, you want to determine whether it is um alkalosis or acidosis. Okay. So the normal range would be between 7.35 to 7.45 K. Now, if it is high, then okay, ankylosis, if it's low acidosis, okay. So now, then you want to look at the carbon dioxide level is carbon dioxide driving the change. If you have low ph with race carbon dioxide, then hopefully that will prompt you to think uh it is a risk territory course. So, therefore, respiratory acidosis, if it is an alkalosis where you have raised ph but low carbon dial site, then again, respiratory course, respiratory alkalosis iss if you have an alkalosis where you have raised ph but raised carbon dioxide. All right. So what is it telling you? It's telling you that the cause is not respiratory, right? It's metabolic and the reason you have the race carbon dioxide is because you're compensating for your metabolic alkalosis. And similarly, if you have acidosis, but your ph is low, what this means is you're compensating for a metabolic acidosis, okay. And then you look at the bicarbonate which will help you tie everything together and confirm whether the carbon dioxide level is compensating for the bicarbonate level or the bicarbonate is or whether it is a respiratory cause? Okay. And is there comp sensation if it is, if your ph is back within the normal range, that it is complete compensation if it is still outside the normal range, but you see either the carbonyl side or bicarbonate level compensating for the other, then it is a partial compensation. Okay. I have a few examples of blood gases because I feel like blood gasses. One of the things where you just need to practice interpreting and hopefully practicing the steps. So number one, what is the Ph? Okay, let's interpret this together. What is the Ph of this? Is this high or low? So let's start with, is this an acidosis or alkalosis ph of 6.9 acidosis or alkalosis? Yes, acid is very good. Okay. In fact, if we look at it. So first of all, before I forget, before we look at the ph actually, the most more thing is look at the blood sample. Is it arterial or is it venous? Okay. And then look at the F I 02 as well. This patient is on 100% oxygen and you're taking an A B G. Usually we don't really take an A B G unless it's a very unwell patient. Okay. So, you know, again, that is already a red flag. So this patient I think is quite unwell arterial blood gas and on 100% oxygen yet there are in profound, profound acidosis or acidemia. Have a look at next, the carbon dioxide level, helpfully, they've given you the normal range. I must say this is not normally uh the um the unit it comes in usually it's kilo pastel, but never mind. Let's look at this anyway. So 100 and 55 is it high or low carbon dioxide, carbon dioxide? 155? And they told you yes, normal range between 35 to 45. So therefore it is high. So you're thinking okay, this is respiratory will likely respiratory acidosis. Now, let's go a step further and look at the bicarbonate level. Okay. The bicarbonate level is 22.5 and 22.5. It's quite, I would say actually it falls within the normal range. So depending on trust, it does vary a little bit. But I would say 22 is is not that low. I would say it's normal actually. So then if the bicarbonate level is normal and your protest and your carbonell says Markley raised and that confirms your diet doses of respiratory acidosis, okay. But let's go a step further and also look at their oxygen level. This is an arterial gas and the patient is on 100% oxygen. Yet the oxygen level here is only 35 you're looking at the normal range of 75 to 100 right? They've drawn arrows to that. They're drawn arrows as well. So they've helped you. 35 is so low for someone on 100% oxygen. So what is this putting things together? Say you want to escalate this patient to a senior or I T U? What would you say this patient has high carbon outside and low oxygen. What is that sort of condition? Exactly? Very good, very good type two respiratory failure. Okay. Type one is where you have uh low oxygen but still normal carbon dioxide level. Type two is when you have raised carbon dioxide level and no uh and low oxygen level. Okay. So causes for type two respiratory failure will be things like pulmonary edema, very common pneumonias and acute exacerbation of COPD in someone who retains carbon outside near fatal asthma or say like an opioid overdose could cause as well. Okay. So type two respiratory failure. Very good. Now the next one. Okay. We don't know. So we need to check the source of this blood gas. We don't know whether as arterial venous, that's fine. Let's look at the ph ph of 7.6. What is that alkalosis or acidosis? Very good ankylosis. Okay. Next, look at the carbon dioxide level. 54 they've given you the normal range 35 45 is the high or low. Yes. Hi. Okay. And then you're like, huh? Ok. High carbon dioxide but it's the patient's alka lot Ick. So what can confirm or what can help confirm the diagnosis whether it is whether it is metabolic alkalosis is looking at the bike up and then you see uh yes, bicarb is 56 then your normal value is like 21 28. So clearly, it's very raised. So in this instants, what happens is um the patient has um also sorry, forgot to point out a base access of 30. All right. So in this case, what it is is a patient with a um metabolic alkalosis iss and some respiratory compensation because you have raised carbon dioxide to offset the raised um bicarb. However, the PH is still well outside your normal range. So what this is is a if you put it in full, partially compensated metabolic ankylosis. Okay. Lovely. Now, last one P H seven point okay. So sample arterial. Yes, F I 02 75. So this patient could potentially be quite unwell ph of 7.295. Is that acidosis or um our kill osis? So below 7.35, then acidosis. Okay. Now, next, we need to look at the carbon dioxide value 63.2, which is well above 45. So it is raised carbon dioxide. Okay. So then yes, it is respiratory acidosis. And then you need to look at the bicarbonate level which sometimes can happen such as in this case is all the way at the bottom. Uh bicarb level is raised as well but not that much raised. Actually, it's only mildly raised So in this instance, what do you think this patient might have? What kind of condition do they have? And also if you notice that oxygen level is also low, so it is again in respiratory failure. But which type, if I don't, then you still see my screen? Okay. Right. So it is in type two respiratory failure, okay. And the reason the bicarb is slightly raised is lightly because this patient could be could be a scenario in a COPD patient and therefore a chronic. So um increase in the bicarb because uh they are compensating for there normal baseline of carbon dioxide level, that's slightly higher than the normal population. Okay. So, but also an example of this type of blood cast where you can see on the wards is say if it is a POSTOP patient, say like day one, post laparotomy and they may have acute respiratory acidosis because of like residual effects of anesthesia. And they might have hypoventilation associated with like post abdominal pain. Therefore, you can see that they're slightly hypoxic. And the reason they're hypoxic is because they are shunting through some atelectatic regions of the lung would basically have lung collapsed from like post abdominal surgery. And then you can have underlying metabolic alkalosis from for example, chronic direct ick use. Okay. So lots of scenarios in where this example for blood gas could happen. But I think it's just learning how to interpret them. Step one ph step to look at carbon dioxide step three, look at bicarbonate level to see if it helps you tie everything together okay. And also look at whether it's arterial or venous right now in how is an eye on gap applicable? It is useful where you have a scenario in which you are not very sure which what is causing that um acid based disturbance make. For example, in this case, it could be a patient with respiratory alkalosis iss and metabolic compensation, partial or you could have mixed respiratory alkalosis with metabolic acidosis because of the low calcium carbon dioxide and low bicarbonate level. How do you know which is which? So the N I on gap is useful in this case because remember the N ion gap is calculated um with this particular equation where you have the positive ions minus the sum of your negative ions. And if your n ion gap is raised, then that's telling you that there are other substances present in the blood. So say in DKA, the patient with a very high anion gap. In which case you would say uh the patient is more likely to be metabolic acidosis rather than the incidence of oh, could it be a mixed respiratory acidosis and metabolical closest, for example? Okay. So and I don't get is useful where you're not very sure what the cause is. If it is Markley raised, then you think that there are foreign exhaustion of substances in the body contributing to the acid based disturbance. It okay and mud plans is just a common pneumonic that people used to think of the causes. Um Yeah, so hopefully that that would be that would come in handy when you're trying to think of horses. Take home message. Always check the source of the blood gas. Whether it's arterial venous arterial usually means the patient's quite unwell or have got some underlying lung pathology and always check the level of oxygenation as well because that will affect your interpretation blood gas values. So say for example, patient is on 100% oxygen and they are just on the borderline um normal within the acceptable range of your 02. Then actually, the patient is still considered to be hypoxic because they're on 100% oxygen. Okay. So that's an example. Always check the level of oxygenation. Good. Well, thank you for sticking with me so far. The last bit is liver function test. It won't, this won't take long at all. So um let's just go through this and then we will finish. Okay. Liver function test. The important thing that you need to distinguish is there are some blood tests that are markers of function of the liver. So actually liver function tests, but there are also other things that come as part of the liver function test confusingly, but rather they're markers of damage rather than markers of liver function. When we talk about liver function, we think of things that the liver actually makes. So things like clotting factors. So therefore the blood test for that would be like a PTT PT or your I am not albumin is also another big one. And Billy Ruben, okay markers of damage it could. Billy Ruben is also a marker of damage A L T A S T in cases where is a viral hepatitis G T, normally alcoholic hepatitis and A LP if it is an obstructive cause. Okay, jaundice in thinking about causes of jaundice, very helpful to classify them into pre hepatic hepatic and post hepatic pre hepatic would be things like to do with the blood. So, um hemolytic anemia where you have increased hemolysis of your heme in your red cells and therefore causing increased bilirubin in hepatic causes. That would normally be liver dis function. So you have um things like viral hepatitis or like drug induced causes and post hepatic that would be obstruction. So, after the biliary tree, so things like Hillary stones or you could have a head of pancreas cancer compressing on the bile duct. And the key in the history for this would be if you have a dark urine and pale stool, okay, raised A L T and A S T. It is quite helpful. Um If you compare the ratios of your A S T two A L T, uh that can help you determine what is the more likely cause for the hepatitis. So, if you're A S T is raised more than you're A L T, then that is more likely to alcoholic. If it is about a ratio of one is to one or if the A S T is slightly less than A L T, that is more likely a viral cause. If it is strong kingly high in the thousands, there are only three causes that could cause that ischemic hit. So is if a patient is profoundly in a profound shock and uh the liver is a scheme ick acute viral hepatitis for toxins like piracy. Two more overdose raised bilirubin. I'm not going to go into like all the details of this. I hope you just know the difference between uncontradicted and conjugated. So, conjugated, conjugation of bilirubin occurs in the liver. So if you have raised uncontradicted bilirubin, so think about prehepatic causes. So raised, increased Hamal icis is one of the biggest causes or impact conjugation. Um JoBeth Syndrome is I wouldn't say relatively common but definitely more common than regular in the jar. Um Don't really need to know those. Um but just know that the difference between uncomplicated and conjugated, conjugated, obviously a lot of different causes. So like if you have liver dysfunction, congenital causes, infections, toxins, etcetera, raised A LP. It is important to remember the LP is produced in different organs, not just the bone, okay. So you also have the placenta, your gi track your kidney and prostate if it is an isolated, raised A LP. Then you need to think about, oh could this be a physiological cause where it is pregnancy because it's produced by Percenter or in Children where they have growth spurts released by the bones. So, therefore, could be physiological or pathological causes. So like math static um cancers that spread to bone, raised G T and A LP, mainly obstructive causes. So, gallstones, very common drugs like amoxiclav that can induce. Um So Cola stasis. So things are called amoxiclav. Um your oral contraceptive pills and alcoholic appetite iss, arrange a LFTs. Um So I wouldn't worry too much about remembering this, but essentially Cola stasis, you always have raised A L P. Um and alcohol abuse, you will have raised G T and in cirrhosis depending on whether they're already at the very end stage of it. You could still have normal clotting actually in cirrhosis or you could have normal uh markers of liver damage as well like A S T and A L T. But if it's the end stage, then your clotting could be deranged album. It could be low and your A S T A L T could be raised the take home message, the best marker of liver function in acute liver injuries, that prothrombin time because that is a, your clotting factors are produced by the liver. So, therefore, it is a function of the liver. If a patient has raised a LP, make sure to check your G T to ensure that it is a bill a resource because A L P raised A LP can also be caused by many other different organs. Okay. So G G T will confirm that it's a bit of resource and um that's it. Thank you very much for listening to my lecture. These are some of the resources that I think um hopefully will be helpful for your um path exam. Definitely the path guide, very, very helpful and I'm sure this pathology lecture series um they were definitely helpful to me. So I hope they've been helpful to you. They're helpful to you too, practice questions. There is this question bank that's produced by some of the seniors. The alumni in the year above us is Met Gems. I'm not entirely sure whether the website still working, it might be, but it's a free resource is definitely check that out and that's pretty good. Um There is a, a book S B S E M T s and clinical Pathology. Um I find the explanations for this book very, very good. So I would definitely try to do some of the questions if you have time and some of the blackboard quizzes, they might be some of them admire. They were a bit out of date, but they might have been updated for your year. Definitely do those. Okay. And thank you very much for your attention. Um Please fill in feedback that would be much appreciated. Any, any questions feel free to either ask in the chat now or you could you know me if you like? Thank you. Perfect. Thank you Nicole for that fantastic lecture. I think what's really nice actually is that you had the C P Q questions? Like I, I don't know if you had this but we, we didn't have much exposure. We haven't so far have much exposure to that. I think it's quite nice to sort of start to practice getting used to them, which is nice for students. Um I'll just quickly share my screen as well if people want to um scan feedback from uh it's been a bit slow. Otherwise the, the link is in the chat. If you guys have any questions, please do ask them now. But genuinely like Campath, I find it's actually one of the nicer uh path topics to study just because it's so like, and especially if you're on the wards, you know, a lot you can like interpret and like practice thinking about, you know, how to deal with the electoral imbalances and stuff nicer than micro with my, my opinion. Yeah. Uh And everyone can just scan that and fill it out. We'd really appreciate it. You guys um Any questions Nicole is only here by here once a year. So another chance guys. Well, if there's no, oh we got a question actually. Yeah. Why are cortisol levels checked in hypercalcemia? Uh Let me think Cortisol levels. Let me go back to my slides. Uh, just give me one second. Mhm. Where have I written that? Mhm. Okay. Um, so if you're thinking of like your men's syndrome, right? Your cortisol levels, um, can be raised in. Actually let me check. Sorry, men one and men too syndrome meant to a, I always forget what the different. Yeah. So in men too, you can have tumors in your adrenal gland. So you want to check the cortisol level to make sure it's not raised as well too. Um Just to make sure that it's not part of the men's syndrome. In which case, that will need referral to like your um endocrine surgeons for further investigation, but it's not something that is routinely checked just to clarify. Um You would definitely do other things like myeloma screen, which is way more common. Um And then your bone profile cortisol is just like an extra thing if you're thinking men's syndrome of it. Well, if there's no more questions, guys, I hope everyone has a lovely evening. And again, thank you so much, Nicole forgetting the next enjoy your weekend. Um It's Easter weekend. So everyone enjoy and yeah, and actually, you know what, just to encourage you a lot when I did path in fifth year, I'm like, this is so much content. So impossible to study. How do I remember everything? But actually when you come to F one F two, you're like, there's so much path knowledge that's so useful. So, hopefully this would, like, help encourage you as you, like, study. It's actually really useful even now. Like, I still think about the path lectures when I try to deal with problems, some medical problems. Yeah. Yeah. Literally I would think of like Amir Sam's voice, Mirren's voice. And, uh, yeah, also you guys are almost at the end and finally it would be really nice. Yeah. Totally onto that. Yeah.